Pocket Emergency Medicine (Pocket Notebook Series) 3rd Ed.

ALLERGIC/INFLAMMATORY EXANTHEMS

Psoriasis

Definition

• Genetic, chronic, inflammatory multisystem disorder affecting primarily skin & joints

• Common, affecting 2% of population

• Majority of pts have mild to moderate dz, thus tx can be initiated if identified in the ED

• May be a/w other inflammatory disorders such as psoriatic arthritis, IBD, & CAD, diabetes, & lymphoma

• Marked by characteristic skin manifestations that wax & wane; environmental triggers include medications, skin trauma, infection, physiologic/psychologic stress

• Phenotypic classifications include plaque (most common), inverse, erythrodermic, pustular, guttate, nail dz (onychodystrophy) & arthritis

History

• Pruritus, pain over fissures

• Assess recent strep pharyngitis, viral URI, immunization, new meds, skin trauma

Physical Findings

• Plaque psoriasis: Well-defined round to oval-shaped scaling, silver papules & plaques on erythematous base mainly on extensor surfaces of extremities (knees, elbows)/scalp/trunk and buttocks; painful fissuring may develop; tends to be symmetric

• Inverse psoriasis: Erythematous plaques w/ minimal scale w/i skin folds, predominant in axilla, inframammary, groin, perineum, intergluteal

• Erythrodermic psoriasis: Generalized erythema covering nearly entire BSA w/ varied scaling; may be a/w fever & malaise

• Pustular psoriasis: Marked by cutaneous pustules on erythematous base

• Guttate psoriasis: Dewdrop-like, 1–10 mm salmon colored papules w/ fine scaling; may be preceded by URI w/ group A β-hemolytic streptococci

• Psoriatic onychodystrophy: Nail dz common in all subtypes; involves nail pitting, onycholysis, & subungal hyperkeratosis

Treatment

• Nonmedications: Daily sun exposure, sea bathing, topical moisturizers

• Options include topical steroids, UVB, PUVA (psoralen plus UV-A), immunosuppressives (methotrexate, CyA), acitretin, biologic agents (alefacept, efalizumab, adalimumab, etanercept, infliximab)

• Topical therapies often can be initiated in ED either as primary therapy for mild dz or adjunctive therapy for those w/ severe dz on other systemic therapy; txs:

• Corticosteroids (midhigh potency 1–2 times daily; optimal end point unknown)

• Vit D analogs (calcipotriene twice daily to affected area) w/ corticosteroid

• Topical emollients or Aloe vera 1–3 times daily

• Other: Tazarotene, salicylic acid, coal tar, anthralin, tacrolimus/pimecrolimus

Disposition

• Home w/ dermatology f/u

Erythema Nodosum

Definition

• A cutaneous reactive process marked by panniculitis that may be triggered by a wide variety of possible stimuli: Infection, sarcoid, rheumatologic dz, IBD, medications (esp sulfa & OCPs), autoimmune disorders, pregnancy, & malignancy among others

• There is an association b/w GAS infection & erythema nodosum, usually w/ onset of rash 2–3 wk after throat infection

• Pathogenesis thought to result from cutaneous rxn from immune complex deposition in an around venules of connective tissue septa of subcutaneous fat leading to acute inflammation of the connective tissue surrounding subcutaneous adipose tissue

History

• Can occur at any age, but usually 2nd & 3rd decades; >F:M

• H/o recent sore throat/URI, or PMH/FH of connective tissue, rheum, autoimmune, or inflammatory bowel dz; review current & new meds

• Pts typically present w/ pain & erythema over anterior tibial region

• May be a/w fever, fatigue, malaise, arthralgia, HA, GI complaints, URI

• Usually lasts 3–6 wk & is self-limited; may recur

Physical Findings

• Erythematous tender, warm nodules & plaques located predominantly over the extensor aspects of the lower extremities (knees, anterior tibial surface, ankles)

• Subacute lesions become flat, & deep red or purplish in color & may mimic ecchymosis

Evaluation

• If needed for underlying dz

• CBC, ESR/CRP, CXR (particularly for e/o Tb or hilar adenopathy)

Treatment

• Supportive: NSAIDs, oral corticosteroids in severe cases

Disposition

• Home with/without referral to dermatologist or rheumatologist

Urticaria

Definition

• Urticaria can be acute, chronic (>6 wk), or contact related, & may also occur secondary to physical triggers (dermatographism, cholinergic, exercise induced, pressure, aquagenic, cold, etc.). Special syndromes include urticarial vasculitis & pruritic urticarial papules & plaques of pregnancy (PUPPP).

• Acute urticarial is most common in clinical practice & commonly idiopathic in nature. Precipitants include food, meds (esp β-lactam abx), insect stings, contact w/ external allergens (ie, latex), or parasites

• Mechanisms include IgE mediated (Type I hypersensitivity), direct mast cell degranulation, complement mediated, metabolism of arachidonic acid (ie, ASA, NSAIDs), autoantibodies to the IgE receptor on mast cells (FcΕRI)

• The key mediator of urticarial formation is histamine

History

• Pruritic rash, may have h/o new exposure

• Maximal intensity of pruritus typically occurs in the evening

• Acute urticarial lasts <6 wk & usually resolves w/i 24 h

• May be a/w h/o atopy

Physical Findings

• Pruritic, pink-erythematous edematous plaques often w/ central pallor, ranging in size from a few millimeters to several centimeters in size. They may appear round or irregular in shape & can occur anywhere on the skin.

Treatment

• Avoidance of precipitants if known; counsel that causes are often not found

• Antihistamines H1-blockers (diphenhydramine, hydroxyzine, cetirizine, loratadine, fexofenadine), H2-blockers (cimetidine, ranitidine, famotidine), steroids (prednisone) for refractory cases, TCAs (doxepin) if unresponsive to antihistamines, epinephrine for severe associated rxn

Disposition

• Home

Eczema

Definition

• Eczema represents a group of skin dz marked by skin inflammation (dermatitis) as well as similar phenotypic clinical manifestations: Erythema, pruritus, scaling, fissures, varying degrees of lichenification, & blistering

• Several common types of dermatologic conditions fall under this umbrella term:

• Atopic dermatitis

• Contact dermatitis

• Seborrheic dermatitis

• Dyshidrotic eczema (Pompholyx)

Atopic Dermatitis

Definition

• Chronic, relapsing & remitting skin dz seen in pts w/ h/o or FH of atopy (asthma/allergic rhinitis/food allergies), 60% begins in 1st year of life

• Affects 10–20% of children & 1–3% of adults

• A/w increased serum IgE levels

• Precipitating factors: Temperature, humidity, irritants, infection, foods, allergens, stress

History

• Dry pruritic rash w/ pruritus & chronic or relapsing eczematous lesions w/ typical morphology & distribution in a pt w/ a h/o atopy

Physical Findings

• Intensely pruritic, erythematous papulovesicular lesions a/w excoriations & serous exudate; chronic lesions w/ lichenification, papules, & excoriations

• In infants & young children, characteristically involves face, neck, & extensor surfaces

• In adults, usually localized to flexural folds of extremities

Nummular eczema: Round-to-oval erythematous plaques most commonly found on the arms & legs. Lesions often start as papules, which then coalesce into plaques w/ scale. Early nummular dermatitis lesions may be studded w/ vesicles containing serous exudate.

Treatment

• Principles of therapy include skin hydration, topical anti-inflammatory medications, antipruritic therapy, antibacterial measures, & elimination of exacerbating factors:

Skin hydration: Warm soaking baths for 10 min followed by moisturizer application

Topical corticosteroids: Low-potency corticosteroids for maintenance therapy, intermediate- & high-potency corticosteroids for tx of clinical exacerbation for short course (see table below)

Topical calcineurin inhibitors: Topical tacrolimus, pimecrolimus

Antihistamines: Oral antihistamines for relief of pruritus; topical antihistamines not recommended due to potential for skin sensitization

Prevention: Avoid irritants—soaps, wool, fragrances, chemicals, etc.; humidity control

Disposition

• Home

Guideline: Schneider L, Tilles S, Lio P, et al. Atopic dermatitis: A practice parameter update 2012. J Allergy Clin Immunol. 2013;131:295–9.e1–e27.

Contact Dermatitis

Definition

• Encompasses all adverse cutaneous rxns that result from the direct contact of an exogenous agent to the surface of the skin

• Can be allergic or nonallergic, irritant in etiology

• Allergic forms result from antigens that become immunogenic after conjugation w/ proteins in skin, triggering an inflammatory cascade (ie, plant dermatitis)

• Irritant forms are multifactorial responses that involve contact w/ a substance that chemically abrades, irritates, or damages the skin w/ subsequent inflammation

• Tissue rxns are attributed to cellular immune (Type IV, delayed hypersensitivity) mechanisms

• Common precipitants: Latex, plant substances (Toxicodendron [formerly Rhus]), metals (nickel), cosmetics/personal hygiene products, hair products, sunscreen, & topical medications among others

• Variants: Photoallergic CD, allergic contact cheilitis, allergic systemic CD

History

• Thorough hx surrounding onset: Work hx, exposure to industrial chemicals, exposure to plant substances, new lotions/perfumes/fragrance soaps/detergent/cosmetics/hair products, new jewelry w/ type of metallic substance, etc.

• Pruritic rash often w/ burning or stinging in the area of contact

Physical Findings

• Papulovesicular erythematous rash which may involve varying degrees of lichenification, fissuring, scaling, & excoriation at the site of contact, usually well localized

• Commonly affected areas include eyelids, face, neck, hands/proximal arms, axilla, waste area, anogenital region, & exposed areas of the lower extremities

Evaluation

• Patch testing is the gold standard for identification of a contact allergen, but not performed in the ED, thus may refer to allergist or dermatologist

Treatment

• Identification & avoidance of offending agent

• Symptomatic relief w/ cold compresses, colloidal baths, & emollients

• Topical corticosteroids are 1st-line tx for localized forms. Tx begins w/ high-potency steroids that may be switched to mid- or low-potency as sxs improve (see table below)

• Systemic corticosteroids may be used for extensive or severe cases

• Consider abx if appears superinfected

• Antihistamines are generally ineffective for CD

Disposition

• Home with/without referral to allergist or dermatologist for patch testing

Guideline: American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology. Beltrani VS, Bernstein IL, Cohen DE, Fonacier L. Contact dermatitis: A practice parameter. Ann Allergy Asthma Immunol. 2006;97:S1–S38.

Seborrheic Dermatitis

Definition

• Papulosquamous disorder on the sebum-rich areas (scalp/face/trunk), abnl immune response to nl skin fungus (Malassezia) is proposed etiology

• Common in infants (cradle cap), during puberty & in elderly

• Incidence is high among pts w/ AIDS & Parkinson’s dz

History

• M > W, 20% have h/o dandruff, worse in winter

• May be concomitant w/ other skin dzs including rosacea, blepharitis, & acne

Physical Findings

• Pink-erythematous, oily, flaking patches of skin on scalp/nasolabial folds/eyebrows/ears/chest/flexural areas

Treatment

• Frequent cleansing → reduce oil, keratolytic shampoos (selenium/sulfur/coal tar), topical ketoconazole (reduce fungal load), low-potency corticosteroids

• Scalp lesions: Selenium sulfide 2.5% shampoo (Selsun) twice weekly for 4 wk, zinc pyrithione 1% shampoo (Head&Shoulders) once daily then twice weekly as needed, or ketoconazole 2% shampoo twice weekly for 4 wk. Instruct pts to leave in for 5–10 min before rinsing; selenium & zinc shampoos can be used daily.

• Face & body lesions: Apply hydrocortisone 1% cream once daily for 4 wk; ketoconazole 2% cream QD or BID for 1 mo may also be effective. This can be used in conjunction w/ the shampoos noted above.

Disposition

• Home

Dyshidrotic Eczema (Pompholyx)

Definition

• Vesicobullous disorder involving palmoplantar skin

• It is a subtype of eczema w/ accumulation of edematous fluid in regions w/ a thick epidermis & even thicker overlying horny layer as in the skin of palms & soles

• 2 clinical presentations include vesicular & bullous types

• May be acute, recurrent, or chronic

• Dyshidrosis is a misnomer, as sweat glands are unaffected in this disorder

History

• Pts present w/ pruritus of the palms or soles a/w vesicular or bullous lesions

• Can be a/w atopic dermatitis, contact dermatitis (esp nickel & cobalt), adverse drug rxns, emotional stress or an id rxn in pts w/ tinea pedis

Physical Finding

• Vesicles & bullae on nonerythematous palmoplantar skin, particularly over the lateral aspects of the fingers, palms, & soles

Treatment

• High-potency topical corticosteroids, systemic corticosteroids for severe cases

• Topical calcineurin inhibitors (tacrolimus, pimecrolimus)

Disposition

• Home



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